A predictable loss of renal perfusion, glomerular filtration rate and many of the kidneys' functions -- including the ability to handle sodium -- occurs with increasing age. Hypertension, which is sensitive to sodium intake, also increases in frequency with increasing age. This study is designed to explore the responsible mechanisms for the limited ability of the aging kidney to handle salt, and its relation to the hypertension. Our first hypothesis is that a functional element contributes to the loss of renal perfusion and to the limitation of sodium handling with increasing age. Our second hypothesis is that the intrarenal generation of AII, prompted by afferent arteriolar organic lesions or an increasing frequency of glomerular obsolescence, contributes to a number of the abnormal features of aging including renal vasoconstriction, limited sodium handling, renin suppression, and a limited natriuretic response to atrial natriuretic peptide. Our third hypothesis, based on the first two, is that angiotensin converting enzyme inhibition will increase renal perfusion, restore more normal sodium handling, restore the kidneys' response to atrial natriuretic peptide and prevent the hypertension. Central to our approach is the application of proven methods to provide a rigorous assessment of steady state sodium balance and to assess the determinants of sodium balance in humans. Successful completion of these protocols will provide insight into the pathogenesis of many of the features of aging and a more rational approach to prevention and treatment.